VIM and hepatocellular carcinoma: It is postulated that by suppressing JAK2 phosphorylation, NOT inhibits JAK2/STAT3 signaling, enhances intracellular ROS burst, and destabilizes VIM, Snail, β-catenin, or N-cadherin oncogene interaction with the stemness marker SOX2 or OCT4, thus suppressing tumorsphere formation and oncogenicity and consequently leading to HCC cell death as expressed by upregulated cleaved PARP levels.